The molecular basis for ultraviolet light carcinogenesis is a matter of speculation. Recently, the principal investigator has found that UVL produces dramatic increases in epidermal ornithine decarboxylase (ODC). ODC, which forms putrescine by decarboxylation of ornithine, is the first and probably the rate limiting enzyme in the biosynthesis of the polyamines, spermidine and spermine. The activities of ODC and the levels of its biosynthetic products are elevated in various systems stimulated to proliferate. Furthermore, numerous studies indicate that the polyamine biosynthetic enzymes are implicated in neoplastic growth. For example, application of a potent tumor promoting agent, 12-Otetradecanoyl-phorbol-13-acetate (TPA) to mouse skin lead to more than 250 fold increases in epidermal ODC activity and this phenotypic change is thought to be essential for skin tumor promotion. In view of the potential significance of ODC for growth carcinogenesis, it is proposed to study in greater detail the response of epidermal ODC to UVL. The effects of various drugs which may modify this UVL induced epidermal ODC activity will be examined. It may be possible to use inhibition of UVL induced ODC epidermal activity as a means for screening agents that are protective against UV carcinogenesis. Can studies of UV induced epidermal ODC help to determine which are the least carcinogenic UV light sources for treatment of certain skin diseases, includng psoriasis?